Source:http://linkedlifedata.com/resource/pubmed/id/17114436
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2006-11-20
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| pubmed:abstractText |
CCL21, a lymphatic endothelial cell (LEC)-derived chemokine, and its receptor CCR7 regulate dendritic cell (DC) trafficking to lymph nodes (LN), but it is unclear how CCL21 expression is regulated. Oncostatin M (OSM) is an IL-6-like cytokine synthesized by activated DC and other leukocytes. In vitro, OSM (but not TNF-alpha) stimulated CCL21 mRNA and protein expression by human dermal microvascular EC (DMEC) in an ERK1/2-dependent fashion. Conditioned medium from OSM-treated DMEC stimulated CCL21-dependent chemotaxis of mouse bone marrow-derived DC (BMDC). Cultured BMDC expressed OSM, which was increased with the addition of LPS. Topical application of the contact-sensitizing hapten, trinitrochlorobenzene, resulted in enhanced OSM expression in the skin, whereas cutaneous injection of TNF-alpha did not. Injection of OSM into the footpad increased CCL21 mRNA expression in the draining LN by approximately 10-fold and in mouse skin by approximately 4-fold without increasing CCR7 mRNA. In vitro, OSM increased the permeability of DMEC and lung microvascular EC monolayers to FITC-dextran beads, and, in vivo, it enhanced accumulation of Evans blue dye in draining LN by approximately 3-fold (p = 0.0291). Of note, OSM increased trafficking of BMDC injected in footpads to draining LN by 2-fold (p = 0.016). In summary, OSM up-regulates CCL21 expression in skin and draining regional LN. We propose that OSM is a regulator of CCL21 expression and endothelial permeability in skin, contributing to efficient migration of DC to regional LN.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCL21 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ccl21c protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL21,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC,
http://linkedlifedata.com/resource/pubmed/chemical/Haptens,
http://linkedlifedata.com/resource/pubmed/chemical/Oncostatin M,
http://linkedlifedata.com/resource/pubmed/chemical/Picryl Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
177
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
7665-72
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:17114436-Animals,
pubmed-meshheading:17114436-Blotting, Western,
pubmed-meshheading:17114436-Capillary Permeability,
pubmed-meshheading:17114436-Chemokine CCL21,
pubmed-meshheading:17114436-Chemokines, CC,
pubmed-meshheading:17114436-Chemotaxis, Leukocyte,
pubmed-meshheading:17114436-Dendritic Cells,
pubmed-meshheading:17114436-Endothelial Cells,
pubmed-meshheading:17114436-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:17114436-Female,
pubmed-meshheading:17114436-Flow Cytometry,
pubmed-meshheading:17114436-Haptens,
pubmed-meshheading:17114436-Humans,
pubmed-meshheading:17114436-Lymph Nodes,
pubmed-meshheading:17114436-Mice,
pubmed-meshheading:17114436-Mice, Inbred BALB C,
pubmed-meshheading:17114436-Mice, Inbred C57BL,
pubmed-meshheading:17114436-Oncostatin M,
pubmed-meshheading:17114436-Picryl Chloride,
pubmed-meshheading:17114436-RNA, Messenger,
pubmed-meshheading:17114436-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17114436-Skin,
pubmed-meshheading:17114436-Tumor Necrosis Factor-alpha
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| pubmed:year |
2006
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| pubmed:articleTitle |
Oncostatin M enhances CCL21 expression by microvascular endothelial cells and increases the efficiency of dendritic cell trafficking to lymph nodes.
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| pubmed:affiliation |
Dermatology Branch, Center for Cancer Research, National Cancer Institute, 10 Center Drive, Bethesda, MD 20892, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural,
Research Support, N.I.H., Intramural
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